Abstract
Schizophrenia is a severe mental illness with visual learning and memory deficits, and reduced long term potentiation (LTP) may underlie these impairments. Recent human fMRI and EEG studies have assessed visual plasticity that was induced with high frequency visual stimulation, which is thought to mimic an LTP-like phenomenon. This study investigated the differences in visual plasticity in participants with schizophrenia and healthy controls. An fMRI visual plasticity paradigm was implemented, and proton magnetic resonance spectroscopy data were acquired to determine whether baseline resting levels of glutamatergic and GABA metabolites were related to visual plasticity response. Adults with schizophrenia did not demonstrate visual plasticity after family-wise error correction; whereas, the healthy control group did. There was a significant regional difference in visual plasticity in the left visual cortical area V2 when assessing group differences, and baseline GABA levels were associated with this specific ROI in the SZ group only. Overall, this study suggests that visual plasticity is altered in schizophrenia and related to basal GABA levels.
Highlights
Schizophrenia (SZ) is a severe psychiatric illness with well-documented visual learning and processing deficits [1,2,3], which may be due to alterations in long-term potentiation (LTP)
Given that glutamatergic function is altered in SZ and a previous study by our group in healthy controls showed that glutamine was related to visual plasticity [11], we hypothesized that the relationship between glutamine to visual plasticity would be weaker in adults with SZ compared to healthy controls
We expected the magnitude of the relationship between glutamate and visual plasticity as well as GABA and visual plasticity to be smaller in adults with SZ compared to healthy controls
Summary
Schizophrenia (SZ) is a severe psychiatric illness with well-documented visual learning and processing deficits [1,2,3], which may be due to alterations in long-term potentiation (LTP). Clapp et al adapted a visual plasticity paradigm that employed low and high frequency stimulation known to induce LTP-like changes in rodents and successfully tested the paradigm in healthy adults using EEG and fMRI. In these studies, increased visual evoked potentials [8] or increased fMRI BOLD activation [9] were observed following high frequency stimulation, which was similar to previous animal studies. Cavus et al demonstrated impaired visual cortical plasticity in adults with SZ compared to healthy controls as evidenced by a lack of persistent visual evoked potentials in the visual cortex post-high frequency stimulation [13]. In a study where participants were given D-cycloserine or placebo, exploratory analyses by Forsyth et al [14] showed impaired visual evoked
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